Role of the stringent response in the expression and mechanism of near‐ultraviolet induced growth delay

The near‐ultraviolet (300–400 nm) induced growth delay of Escherichia coli cells was compared in isogenic relA + and relA − cells illuminated either in the stationary or the exponential phase. In the latter case: (a) the relA − strains of K12 and B/r exhibited similar maximal growth lags (65 min and 55 min respectively); (b) the maximal lags were 1.5‐fold and 4‐fold longer, respectively, in the isogenic relA + strains;(c) the rate of the relA − ‐dependent guanosine 3′,5′‐bis(diphosphate) (ppGpp) accumulation was three‐times lower in the K12 relA + strain as compared to the B/r relA − strain: (d) a K12 spoT mutant having an impaired rate of ppGpp degradation had a 2‐fold longer lag. On the other hand, when illumination is performed in the stationary phase, isogenic relA + and relA − cells (B/r or K12) exhibited similar growth lags at any fluences, indicating little if any involvement of the stringent response. These data extend previous observations of T. V. Ramabhadran and J. Jagger [(1976) Proc. Natl Acad. Sci. USA, 73 , 59–63] but do not support their conclusion that the stringent response is the main factor responsible for growth delay. By monitoring the intracellular level of ppGpp in relA + spoT − and relA + spoT + growing cells during illumination and the subsequent growth lag we observed that the initial burst of ppGpp decreases slowly all along the lag; in all relA + strains checked the return of ppGpp to its basal level coincides with the recovery of normal growth. We conclude that it is the accumulation of ppGpp over the basal level due either to the stringent response or to prevention of ppGpp degradation that is responsible for an amplification of the growth lag.